Journal of Pathology and Translational Medicine

Review

Acute Atherosis of the Uterine Spiral Arteries: Clinicopathologic Implications: Joo-Yeon Kim, Yeon Mee Kim; J Pathol Transl Med. 2015;49(6):462-471. Published online November 4, 2015; DOI: https://doi.org/10.4132/jptm.2015.10.23

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Acute atherosis is unique vascular changes of the placenta associated with poor placentation. It is characterized by subendothelial lipid-filled foam cells, fibrinoid necrosis of the arterial wall, perivascular lymphocytic infiltration, and it is histologically similar to early-stage atherosclerosis. Acute atherosis is rare in normal pregnancies, but is frequently observed in non- transformed spiral arteries in abnormal pregnancies, such as preeclampsia, small for gestational age (SGA), fetal death, spontaneous preterm labor and preterm premature rupture of membranes. In preeclampsia, spiral arteries fail to develop physiologic transformation and retain thick walls and a narrow lumen. Failure of physiologic transformation of spiral arteries is believed to be the main cause of uteroplacental ischemia, which can lead to the production of anti-angiogenic factors and induce endothelial dysfunction and eventually predispose the pregnancy to preeclampsia. Acute atherosis is more frequently observed in the spiral arteries of the decidua of the placenta (parietalis or basalis) than in the decidual or myometrial segments of the placental bed. The presence and deeper location of acute atherosis is associated with poorer pregnancy outcomes, more severe disease, earlier onset of preeclampsia, and a greater frequency of SGA neonates in patients with preeclampsia. Moreover, the idea that the presence of acute atherosis in the placenta may increase the risk of future cardiovascular disease in women with a history of preeclampsia is of growing concern. Therefore, placental examination is crucial for retrospective investigation of pregnancy complications and outcomes, and accurate placental pathology based on universal diagnostic criteria in patients with abnormal pregnancies is essential for clinicopathologic correlation.

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Original Articles

Ultrastructural Changes of Lead Acetate Induced Liver Injury in Rats.: Eun Sook Chang, Jin Seok Oh; Korean J Pathol. 1996;30(3):184-198.

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Abstract PDF: To evaluate the ultrastructural changes and the mechanism causing liver injury by lead, light and electron microscopic(LM and EM) examination using Timm sulphide silver method(TSM) was done. Sprague-Dawley rats were divided into a control and 3 experimental groups. The experimental groups were orally administered 0.5% lead acetate(LA). Group 1 received a one time dose of 10 ml of LA by gastric intubation. Groups 2 and 3 continuously received LA instead of drinking water. The control group was composed of 3 rats in each group which did not receive any treatment. Rats of group 1, 2 and 3 and control were sacrificed at 1/2, 1, 1 1/2 hours, 2 days, and at 1, 2, 4, 6 and 8 weeks later, except group 3. Before sacrifice, they were perfused with 0.1% sodium sulphide and 2.5% glutaraldehyde through the abdominal aorta for TSM. The liver was taken for LM and EM examinations. Blood lead concentration began to increase from the 2nd day up to 3.29 microgram/ml at 2nd week, and the urinary delta-ALA level showed a steady increase from the 2nd day. LM and EM examination of liver revealed that absorbed lead granules in group 1 were transported into sinusoidal spaces, Kupffer cells, and the hepatocytes within 1 hour and then disappeared 1/2 hour thereafter. In group 2 deposited lead was found in the hepatocytic cytosol bound to mitochondria. That in turn inhibited mitochondrial respiration with resultant mitochondrial swelling at the 1st week and thereafter at 6th week myelin figure formation and condensation of mitochondria, and peroxisomes were increased at 8th week. Based on these results it can be concluded that a transient intake of subletal dose of LA is biotransformed completely by periportal hepatocytes within 1 1/2 hours, but excessively accumulated lead can induce liver cell injury due to lipid peroxidation of membrane by direct toxic effect of lead and by products of lipid peroxidation. We postulate that lead acetate triggers presumably primarily mitochondrial membrane injury and then other organellar changes may play a role in disturbance of a network of interacting of key events capable of causing cell death.

Clear Cell Islet Cell Tumor of the Pancreas: An Immunohistochemical and Ultrastructural study.: Seung Sam Paik, Young Ha Oh, Eun Kyung Hong, Moon Hyang Park, Jung Dal Lee; Korean J Pathol. 1997;31(2):162-166.

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Abstract PDF: A clear cell islet cell tumor of the pancreas is extremely rare and characterized by extensive clear cell components. Electron microscopic and immunohistochemical findings are essential to prove that the mass with clear cells is an unusual manifestation of an islet cell tumor. Herein, we report a case of clear cell islet cell tumor of a 54-year-old woman with abdominal pain. The tumor was composed of polygonal clear cells arranged in nests, trabeculae, and ribbon pattern with the extensively fibrous stroma. These tumor cells showed strong reactivity for chromogranin and weak reactivity for somatostatin and glucagon. An electron microscope revealed that the important contributing factor of the clear cytoplasmic change was mainly due to an accumulation of lipid droplets, coupled with cytoplasmic swelling in some areas. Some tumor cells showed many endosecretory granules ranging from 111 to 297nm in diameter. In the clinical and immunohistochemical findings these granules were consistent with somatostatin granules in morphology and size.

Experimental Study on Shark Liver Oil-Induced Lipoid Pneumonia in Rats.: Mee Soo Chang, Eui Keun Ham; Korean J Pathol. 1997;31(8):711-722.

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Abstract PDF: The purpose of this experiment is to evaluate the histopathologic findings of shark liver oil-induced lipoid pneumonia, and to determine whether shark liver oil is absorbed through lymphatics and the venous system or not. A single intratracheal administration of shark liver oil (0.6 ml/kg of B.W.) was given to Sprague-Dawley rats. They were then sacrificed sequentially from 1 hour to 12 weeks after injection. We investigated the chest radiographic findings, the serum total lipid concentration of blood obtained by cardiac puncture, lipid-laden alveolar macrophage index of the bronchoalveolar lavage fluid, and the histopathology of tracheobronchial lymph nodes and the lung (Oil red O stain & H&E stain). Chest radiographs showed no specific findings; ill-defined hazy, linear, small patch radioopacity, air space consolidation or collapse. Thirty-six percent of the experimental rats revealed normal findings. Within the lung, the shark liver oil appeared either as highly emulsified fine granules in the cytoplasm of the alveolar macrophage or as free, round oil masses. The area of the lung accumulated with lipid material was maximized 1 week after injection, and then decreased thereafter. The tissue reactions were cuboidal metaplasia of the alveolar lining, widening and lymphocytic infiltration of the alveolar septa and granuloma formation (3% of experimental rats) as a reaction to a foreign body. There were also lung abscesses due to superimposed bacterial infection (5% of experimental rats). With time after the injection of the oil, the serum total lipid tended to increase and the intracellular lipid of the alveolar macrophages in the bronchoalveolar lavage fluid tended to decrease. In summary, the histopathologic findings of the lung in the experimental lipoid pneumonia were interstitial chronic inflammation and granulomas with the presence of lipoid material in the lung parenchyma, and shark liver oil appeared to be absorbed in the blood and the lymph, then metabolized.

Ultrastructural Study of Amiodarone-Associated Lung Injury.: Eun Yung Kim, Sang Han Lee, Yoon Kyung Sohn, Tae Joong Sohn; Korean J Pathol. 1995;29(1):10-23.

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Abstract PDF: Amiodarone, an antiarrhythmic drug, may exert pulmonary toxicity in some patients but the pathogenesis is not clear. This study was carried out to investigate the pathogenetic mechanism of pulmonary injury induced by amiodarone at dose of 100 mg/kg/day given to rats by intraperitoneal injection for 3 weeks. And the preventive effects of concomitantly injected steroid (10 mg/kg/day) on amiodarone induced pulmonary injury was also studied using bronchoalveolar lavage, light microscopy and transmission electron microscopy. The results obtained were summarized as follows: Mild lymphocytosis of bronchoalveolar lavage fluid was found in all experimental groups. Intracytoplasmic lamellar body formation was found in all types of pulmonary cells and type II pneumocytes revealed the earliest abnormal lamellar body formation. The capillary endothelial cells showed cellular swelling and detachment from underlying basement membrane at early phase of experiment and the edema of alveolar wall and interstitium were noted. Interstitial fibrosis and proliferation of type II pneumocytes were noted at late phase. The lungs of steroid injected groups revealed accumulation of lamellar bodies in all types of pulmonary cells but interstitial fibrosis was not occurred. These findings support the concept that amiodarone is responsible for a drug-induced phospholipidosis and directly toxic to pulmonary endothelial and epithelial cells. And steroid may regress the progression of amiodarone induced pulmonary injury.

Phospholipidosis of Liver Induced by Amiodarone.: Dong Hoon Kim, Gium Mi Jang, In Soo Suh, Tae Joong Sohn; Korean J Pathol. 1991;25(1):1-10.

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Abstract PDF: Ultrastructural study of the effects of amiodarone on the liver tissue was performed. Rats were fed with amiodarone containing diet and were sacrificerd at 1st, 3rd, 4th, 5th and 8th weeks of experiment. Charateristic lisosomal inclusion bodies were appeared form first week, which were more prominent and increased in size at the 5th and 8th week of experiment. These inclusion bodies were found in hepatocytes, Kupffer cells, bile duct epithelial cells and fibroblasts but most prominent in hepatocytes. The lysosomal inclusion bodies could be divided into four types; those characterized by (1) dense bodies with packed crystaloid contents, (2) multilamellated bodies, (3) irregular shaped bodies with varying electron density and 4. dense bodies containing stacks of fine membranous structures. All types were found in all experimental groups. But the type 1 and 2 were predominent at early stage, while type 3 and 4 were more prominent at later stage According to these findings, the formation of the lysosmal inclusion body was a characteristic change in derangement of phospholipid metabolism. And amiodarone could induce disturbance of phospholipid metabolism in all kinds of cells in liver tissue.

Case Report

Lipid Cell Tumor of the Ovary: A case report.: Sung Churl Lim, Keun Hong Kee, Ho Jong Chun, Hae Sook Song, Chae Hong Suh; Korean J Pathol. 1989;23(1):181-186.

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Abstract PDF: Lipid cell tumors of the ovary are among the rarest of the functional ovarian neoplasms. Recently, authors experienced a case of lipid cell tumor of the left ovary in a 19 year old female, who presented with amenorrhea and hirsutism for 4 years. Grossly, the ovary was well encapsulated, and measured 6.5x6x4.5 cm. Cut surface show homogenous yellowish bulging neoplastic tissue and peritheral displaced normal ovarian tissue. Microscopically, neoplastic cells were composed of rounded and polyhedral cells, arranged in nests seperated by rich vascular networks. On the basis of the author's findings and the evidence available in the literature, we determined this case as ovarian lipid cell tumor.

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